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Biomedical subjects

H Kannan

Publications and source records attributed to H Kannan.

At least 19 recordsLinked to original sources
PubMed1994

Effects of centrally administered endothelin-3 on renal sympathetic nerve activity and renal blood flow in conscious rats.

Effects of intracerebroventricular (i.c.v.) administration of endothelin-3 (ET-3) on renal sympathetic nerve activity (RSNA) and renal blood flow (RBF), arterial blood pressure and heart rate were examined in conscious rats. Administration of ET-3 (1-50 pmol) through a chronically implanted cannula evoked an increase in arterial blood pressure and decreases in heart rate and RSNA, whereas RBF measured by Doppler flow probes did not change. Maximum changes in these responses occurred 10-15 min after i.c.v. administration of ET-3 and the responses returned to the control level after approximately 60 min. In sinoaortic denervated (SAD) rats, the decrease in RSNA induced by i.c.v. ET-3 was attenuated but still significantly persistent. During the experiments, we found that the injection of ET-3 (50-100 pmol) induced a barrel rotation, with an onset latency of 10-15 min. In those cases, prominent increases in arterial blood pressure and RSNA were observed, and these lasted for more than 60 min. The result shows that ET-3 can have centrally mediated effects on autonomic nerve activity as well as on cardiovascular function.

Animals↗
PubMed1993

Synaptic inputs from the stomach to tuberoinfundibular neurons in the paraventricular nucleus of the hypothalamus in rats.

In male rats anesthetized with urethane (600 mg/kg) and alpha-chloralose (60 mg/kg), extracellular recordings were made from tuberoinfundibular (TI) neurons in the paraventricular nucleus (PVN) identified by antidromic stimulation of the median eminence. Electrical stimulation of the gastric branches of the vagus nerve excited 26 (72%) of 36 TI neurons tested. I.v. (0.5-1 microgram/rat) or i.p. (5 micrograms/rat) administration of cholecystokinin (CCK-8) excited 10 (63%) of 16 TI neurons tested. The excitatory responses induced by CCK-8 were abolished by bilateral cervical vagotomy. These results suggest that TI neurons in the PVN receive excitatory inputs from gastric afferents via vagus nerves.

Animals↗
PubMed1993

CCK-8 excites oxytocin-secreting neurons in the paraventricular nucleus in rats--possible involvement of noradrenergic pathway.

Systemic administration of CCK-8 increased plasma oxytocin (OXT) level in rats anesthetized with a mixture of urethane and alpha-chloralose. Extracellular recordings were made from magnocellular neurosecretory neurons in the paraventricular nucleus (PVN) of the hypothalamus in anesthetized rats to examine the effects of CCK-8 on the firing of PVN neurons. Thirteen out of 16 nonphasic neurons (putative OXT-secreting neurons) were excited by intravenous and/or intraperitoneal administration of CCK-8. By contrast, 8 out of 10 phasic cells, vasopressin(AVP)-secreting cells, were inhibited by systemic administration of CCK-8. Four out of five nonneurosecretory neurons in the PVN were excited by the administration of CCK-8. Moreover, microiontophoretically applied phentolamine blocked the excitatory responses induced by CCK-8 in nonphasic neurons. We measured extracellular noradrenaline (NA) level in the PVN, using in vivo microdialysis. Intravenous administration of CCK-8 induced NA release in the PVN. These results suggest that CCK-8 activates the excitatory afferent pathway to putative OXT-secreting neurons in the PVN which may, at least in part, be involved in the central noradrenergic projection.

Adrenergic Antagonists↗
PubMed1993

The actions of endothelin on single cells in the anteroventral third ventricular region and supraoptic nucleus in rat hypothalamic slices.

Endothelin (ET), a peptide consisting of 21 amino-acid residues was recently isolated from the culture supernatant of porcine aortic endothelial cells. ET has been reported to be a more potent vasoconstrictor than angiotensin II. Other studies suggest that ET is involved in central control of the autonomic nervous system and body water regulation. Extracellular recordings were made from neurons in the anteroventral third ventricle (AV3V) and supraoptic nucleus (SON) in rat hypothalamic slice preparations. ET-3 was applied at concentrations of 10(-10) M to 3 x 10(-7) M. Of 226 AV3V neurons tested, 48 (21%) were excited, 8 (4%) were inhibited, and 170 (75%) were unaffected by ET-3 at 10(-7) M. The threshold concentration to evoke the responses was approximately 10(-9) M. Of 144 SON neurons tested, 64 had a phasic firing pattern and 80 had a non-phasic firing pattern. Of 64 phasic neurons tested, 39 (61%) were inhibited by ET-3 at 10(-7) M, 25 (39%) were non-responsive and none was excited. Of 80 non-phasic neurons tested, 14 (17.5%) were inhibited by ET-3 at 10(-7) M, 66 (82.5%) were non-responsive and none was excited. The effects of ET-1 were compared with those of ET-3. The number of neurons responding to ET-1 and their responsiveness were almost the same as for ET-3. To investigate whether the ET responses are dependent on Ca2+ influx, a Ca2+ free medium and the Ca2+ antagonist, nicardipine, were used. The excitatory responses of AV3V neurons to ET were maintained in the Ca2+ free medium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Inward sodium current involvement in regenerative bursting activity of rat magnocellular supraoptic neurones in vitro.

1. The rat hypothalamic slice preparation was used to investigate the involvement of inward Na+ currents as well as inward Ca2+ currents in the generation of bursting activity by supraoptic (SON) neurones. Intracellular records were made from thirty-two SON neurones which showed regenerative bursting activity. The bursting activity consisted of spontaneous, intermittent bursts of action potentials with subsequent silent periods. During the bursts, plateau potentials on which action potentials were superimposed were frequently observed. 2. Perfusion of a low-Na+ medium, a tetrodotoxin (TTX)-containing medium or a Ca(2+)-free medium suppressed the regenerative bursting activity. 3. Addition of 3-10 microM veratridine to Ca(2+)-free medium elicited regenerative bursting activity and spontaneous plateau potentials. The veratridine-induced regenerative bursting activity and plateau potentials were blocked by 1 microM TTX. Addition of 5 mM TEA allowed regenerative bursting activity to persist in Ca(2+)-free medium. 4. These results suggest that TTX-sensitive Na+ inward currents as well as Ca2+ inward currents contribute to the generation of bursting activity in rat SON cells.

Animals↗
PubMed1992

Intraperitoneal administration of recombinant human interleukin-1 beta inhibits osmotic thirst in the rat.

Decrease in water intake after intraperitoneal injection of interleukin-1 beta (IL-1 beta) was studied in the rat. Administration of IL-1 beta at a dose of 20 micrograms/kg attenuated osmotic thirst induced by intraperitoneal injection of hypertonic saline, but did not affect hypovolemic thirst induced by subcutaneous injection of either polyethylene glycol or angiotensin II. Interleukin-1 beta also decreased spontaneous intake of water but not that of 1.8% saline. The results suggest that the decrease in water intake by IL-1 beta is caused, at least in part, by suppression of osmotic thirst but not by general suppression of behavior. The effects of IL-1 beta were not secondary responses accompanied by feeding behavior, since food supply was removed during the experiments. Pretreatment with indomethacin blocked the decrease in water intake by IL-1 beta, suggesting the involvement of production of prostaglandins.

Angiotensin II↗
PubMed1992

Excitation of hypothalamic paraventricular neurons by stimulation of the raphe nuclei.

Extracellular recordings were made from 467 anti-dromically identified neurosecretory neurons and 148 non-neurosecretory neurons in the paraventricular nucleus of the hypothalamus of hemispherectomized cats under pentobarbital anesthesia. Stimulation of the dorsal, median, and pontine raphe nuclei excited 31%, 26%, and 12% of neurosecretory neurons tested, respectively, and inhibited 9%, 7%, and 8%. The excitatory responses in 13 of 14 neurons tested were blocked by either of two intravenously administered 5-HT2 antagonists, cyproheptadine or methysergide. The 5-HT1A antagonist, (-)pindolol, partially blocked the excitatory responses elicited by raphe stimulation in three of five neurons tested. The inhibitory responses to raphe stimulation were not affected by application of these antagonists. More non-neurosecretory neurons than neurosecretory neurons were excited in response to raphe stimulation and these excitatory responses were also blocked by these antagonists. We conclude that most electrically stimulated synaptic inputs from the midbrain raphe nuclei to the hypothalamic paraventricular nucleus are excitatory and are mainly mediated by 5-HT2 receptors.

Animals↗
PubMed1992

Interleukin-1 beta directly excites hypothalamic supraoptic neurons in rats in vitro.

Responses of 42 neurosecretory neurons in the supraoptic nucleus (SON) to human recombinant interleukin-1 beta (IL-1 beta) were examined during intracellular recordings in rat brain slices. IL-1 beta (10(-9)-10(-8) M) depolarized the membrane and caused increased firing in 25 neurons (59.5%). In 11 other neurons (26.6%), depolarization was also seen, followed by membrane hyperpolarization. The IL-induced depolarizing effect remained in the presence of tetrodotoxin (TTX) but was abolished by sodium salicylate. The results suggest that IL-1 beta mainly exerts a direct excitatory effect on SON neurons and further, that prostaglandins may be involved in such an effect.

Animals↗
PubMed1991

Effects of centrally administered angiotensin on sympathetic nerve activity and blood flow to the kidney in conscious rats.

The effects of intracerebroventricular (i.c.v.) administration of different doses (10 pg-100 ng) of angiotensin II (AII) on renal sympathetic nerve activity (RSNA), mean arterial blood pressure (MAP), heart rate (HR), renal blood flow and femoral blood flow have been examined in conscious rats. Administration of AII (10 ng) through a chronically implanted cannula induced an increase in MAP (20-22 mmHg), a decrease in HR (24 bpm), a decrease in RSNA by 57%, a decrease of femoral blood flow by 21% but no change in renal blood flow. The effects on MAP, HR and RSNA are greatly attenuated by the prior i.c.v. injection of an AII-antagonist saralasin. In anesthetized rats, renal denervation significantly attenuated an increase in urinary sodium excretion induced by i.c.v. injection of AII. Since activation of the renal nerve is known to induce sodium reabsorption from the renal tubule and renin release, the relevance of the present finding is discussed in relation to the effect of AII on sodium excretion.

Angiotensin II↗
PubMed1991

Gastric afferents to the paraventricular nucleus in the rat.

Extracellular recordings were made from vasopressin (AVP) and oxytocin (OXT)-secreting cells in the paraventricular nucleus (PVN) of the hypothalamus in rats anesthetized with urethane-chloralose to determine the effects of electrical stimulation of vagal gastric nerves and gastric distension on their activity. Electrical stimulation of gastric branches of the vagus nerves inhibited 5 and excited 10 of 32 phasically firing neurosecretory cells. Approximately one third of the phasically firing neurosecretory cells (9 out of 29 cells) were transiently inhibited by gastric distension; an effect which was completely abolished by bilateral cervical vagotomy. In contrast, gastric nerve stimulation excited 45 of 72 non-phasically firing paraventricular cells. Thirteen of 77 non-phasically firing cells tested were excited by gastric distension. We conclude that there are some sensory afferent inputs originating from gastric receptors and transmitted by gastric vagal afferents which inhibit the activity of AVP-secreting neurons in the PVN although other inputs excite the cells. Similar inputs also excite some of the putative OXT-secreting neurons in the PVN.

Animals↗
PubMed1991

Endothelin-3 directly affects neurons in the anteroventral third ventricle region and supraoptic nucleus of the rat hypothalamus in vitro.

Extracellular recordings were made from anteroventral third ventricle (AV3V) and supraoptic nucleus (SON) neurons of rat hypothalamus in slice preparations. ET-3 was applied at concentrations of 10(-10) to 3 x 10(-7) M. Of 119 AV3V neurons tested, 21 (18%) were excited, 8 (6%) were slightly inhibited, and 90 (76%) were unaffected. The threshold concentration to evoke responses was approximately 10(-8) M. Excitatory responses of the AV3V neurons to ET-3 remained in a Ca(2+)-free medium. Of 120 SON neurons tested, 46 were phasic (putative vasopressin neuron) and 74 were nonphasic (putative oxytocin neuron). Of 46 phasic neurons tested, 26 (56.5%) were inhibited by ET-3, 20 (43.5%) were nonresponsive, and none was excited. Of 74 nonphasic neurons tested, 14 (19%) neurons were inhibited by ET-3, 60 (81%) were nonresponsive, and none was excited. These results suggest that ET-3 has dual effects on AV3V and SON neurons and the mechanisms of the responses may be different in the AV3V and SON neurons.

Animals↗
PubMed1990

Effects of centrally administered atrial natriuretic polypeptide on sympathetic nerve activity and blood flow to the kidney in conscious rats.

Effects of intracerebroventricular (i.c.v.) administration of atrial natriuretic polypeptide (ANP) on renal sympathetic nerve activity (RSNA) and renal blood flow (RBF) were examined in conscious rats. Administration of ANP had no appreciable effects on baseline RSNA and RBF. The pressor response induced by i.c.v. angiotensin II (AII) was attenuated by prior i.c.v. administration of ANP but no significant effect of ANP was observed on the AII-induced bradycardia and inhibition of RSNA. The result shows that centrally administered ANP has little effect on basal RSNA and RBF but it antagonizes the pressor response caused by AII without affecting induced changes in heart rate and RSNA.

Action Potentials↗
PubMed1990

Osmotic responses of rat paraventricular neurons by pressure ejection method.

Extracellular recordings were made from 44 spontaneously active neurosecretory and 43 unidentified neurons in the paraventricular nucleus (PVN) of the hypothalamus in urethane-anesthetized rats. Physiologically hypertonic (+30 mOsm/kg, NaCl or mannitol) and hypotonic (-30 mOsm/kg) solutions were applied by pressure through multibarrel micropipettes to the immediate vicinity of neurons. Of 44 neurosecretory neurons tested, 31 (70%) were unaffected by locally applied osmotic stimulation, and the remaining 13 were excited. Of these 31 osmotically unresponsive neurosecretory neurons, 21 were further tested with very strong hypertonic (+260 mOsm/kg, NaCl) solution, and only 7 were affected. Of 43 unidentified neurons, 28 (65%) were unaffected by osmotic stimulation, and 12 were excited. Accordingly, only parts (30%) of both the neurosecretory and unidentified neurons in the PVN were found to be osmosensitive. We concluded that some neurons in the rat PVN are osmosensitive and osmosensitivity is not specific to neurosecretory neurons in the PVN.

Action Potentials↗
PubMed1989

Inhibition of renal sympathetic nerve activity of anesthetized rats by intracerebroventricular administration of angiotensin II.

Effects of intracerebroventricular (i. c. v.) administration of angiotensin II (AII) on renal sympathetic nerve activity (RSNA), arterial pressure, and heart rate were examined in rats anesthetized with a mixture of urethane and alpha-chloralose. Administration of AII evoked an increase in arterial pressure and a decrease in RSNA with no significant change in heart rate. Prior i. c. v. administration of an AII antagonist, saralasin, greatly attenuated the pressor response and inhibition of RSNA induced by i. c. v. AII. Rats with sinoaortic denervation showed the same magnitude pressor response and decrease in RSNA as intact animals. The result suggests that central AII directly inhibits RSNA via AII specific receptors.

Action Potentials↗
PubMed1989

Activity of hypothalamic neurons in conscious rats decreased by hyperbaric environment.

Single-unit activity of neurons in rat hypothalamus, prefrontal cortex (PFC) and central medial thalamus (CM) was recorded through chronically implanted electrodes. Upon being subjected to 7 atmospheres absolute (ATA) hyperbaric air (709 kPa) environment, about two-thirds of the hypothalamic neurons tested reversibly decreased their firing rate to 71 +/- 12% (mean +/- SD, n = 25) compared to the precompression control activity, and the remaining one-third did not change their firing rate (100 +/- 6%, n = 13). It is suggested that the decrease in firing rate was attributable to increased partial pressure of both oxygen and nitrogen. In contrast to the hypothalamus, the firing rates of most neurons in the PFC and CM did not decrease (99 +/- 9% for PFC, 107 +/- 12% for CM). In separate acute experiments, 3 out of 5 hypothalamic neurons tested in the isolated forebrain also decreased their firing rates in hyperbaric environment. The results suggest that the hyperbaric air acted directly on the forebrain and depressed more than half of the hypothalamic neurons.

Action Potentials↗
PubMed1989

Involvement of caudal ventrolateral medulla neurons in mediating visceroreceptive information to the hypothalamic paraventricular nucleus.

Both neurohypophyseal and tuberoinfundibular neurosecretory neurons in the PVN received excitatory synaptic inputs from the CVLM. We electrophysiologically identified neurons in the CVLM which project to the PVN. On the basis of antidromic spike latencies, two different populations of neurons could be differentiated: slow- and fast-conducting cells. Slow-conducting cells which were presumed to be A1 catecholaminergic cells, received inhibitory and excitatory synaptic inputs from arterial baroreceptors and the cervical vagus nerve, respectively. Our results suggest that slow conducting cells in the CVLM which cause excitation of PVN neurons via a monosynaptic pathway, mediate visceroreceptive information to the PVN.

Afferent Pathways↗
PubMed1989

Increase in sympathetic outflow by paraventricular nucleus stimulation in awake rats.

Our previous studies demonstrated that stimulation of the hypothalamic paraventricular nucleus (PVN) in anesthetized rats evoked a depressor response accompanied with a decrease in sympathetic outflow (H. Kannan, A. Niijima, and H. Yamashita, J. Auton. Nerv. Syst. 19: 83-86, 1987; H. Yamashita, H. Kannan, M. Kasai, and T. Osaka, J. Auton. Nerv. Syst. 19: 229-234, 1987). Because anesthesia may alter cardiovascular responses, we examined in conscious rats the effects of PVN stimulation on arterial pressure, heart rate, and renal sympathetic nerve activity. Electrical stimulation through chronically implanted electrodes evoked increases in arterial pressure and renal sympathetic nerve activity with a slight decrease in heart rate. The magnitude of responses was dependent on the frequency and the intensity of the stimulus. Latency of the excitatory response of the renal sympathetic nerve activity was approximately 70 ms. Microinjection of L-glutamate (0.5 M, 200 nl) into the PVN area also elicited increases in blood pressure and renal sympathetic nerve activity. These results suggest that activation of PVN neurons in conscious rats produces pressor responses due to an increase in the sympathetic outflow. These findings contrast with those obtained previously in anesthetized rats.

Action Potentials↗